On the other hand, inhibition of HIF-1α activity by HIPK2 reduces VEGF, MDR1, and Bcl2 expression and stimulates drug-induced apoptosis in p53-dependent and-independent ways [18], providing a rationale for the potential use of HIPK2 transduction or restoration of HIPK2 function to inhibit HIF-1 pathway and sensitize chemoresistant tumor cells to drugs. Here, BCL2 is linked to neoplasm.